Long-term treatment with nitrates increased cardiac events in patients with healed myocardial infarction.

cute aortic dissection presents with various symptoms; that is, pain, nausea, vomiting, hematemesis, cold sweat, syncope, cerebrovascular accident, ischemic peripheral neuropathy, hypertension, congestive heart failure, shock, cardiac arrest, and sudden death. In addition, fever is often associated with acute aortic dissection and in rare cases is persistent so that it becomes difficult to determine whether or not it is associated with acute aortic dissection. A number of such cases have been reported, 1-4 as well as those in which aortic dissection was identified as the cause of an initially unexplained fever. [5][6][7][8][9][10] However, the duration of fever associated with acute aortic dissection is not well known, so the present study was undertaken to investigate the duration of fever associated with acute aortic dissection and to examine the relationship between duration and hematological parameters and reduction in false lumen size. Methods SubjectsDuring the 26-year period from January 1978 to December 2003, 336 patients with acute aortic dissection were admitted to Kinki University Hospital. Of these 57 meeting the following requirements were selected: (1) hospitalization within 1 week after disease onset, (2) treated medically rather than surgically, (3) judged free of infection, ileus, acute renal failure, malignant tumor, collagen disease, drug allergy, etc and (4) followed for 1 month after disease onset. Diagnosis of DissectionContrast-enhanced computed tomography (CT) scans were used to make a definitive diagnosis of aortic dissection. FeverAxillary body temperatures were measured and the highest temperature during the day was considered the body temperature for that day. A diagnosis of fever was made if body temperature was over 37°C. The duration of fever was defined as the period from the onset of fever to the last day on which body temperature was over 37°C during the 1-month follow-up period.The mean duration of fever was calculated for the entire study population. The patients were then divided into 2 groups: those with duration of fever shorter than the mean (Group A: brief fever group) and those with duration of fever equal to or longer than the mean (Group B: extended fever group). Hematological parameters and reduction in false lumen size were compared between these groups. Reduction in False Lumen SizeContrast-enhanced CT images, obtained at admission and 1 month later, were fed into a computer to determine the false lumen reduction ratio, as shown in Fig 1. HematologyWhite blood cell (WBC) and platelet counts, and C-reactive protein (CRP), fibrinogen, fibrin degradation product (FDP), D-dimer, and thrombin -antithrombin III complex (TAT) concentrations were compared between groups. Mean values for the WBC and platelet counts and CRP concentration were calculated for each week, and changes were analyzed at 1, 2, 3 and 4 weeks after admission. For fibrinogen, FDP, D-dimer, and TAT, the means weeks 1-2 and weeks 3-4 were analyzed.Circ J 2007; 71: 766 -771 (Received September 4, 2006; ...

This study showed that use of short-acting nifedipine and diltiazem in this postmyocardial infarction population was associated with a 24% higher cardiac event rate, but this strong adverse trend did not reach statistical significance.

To investigate the aldosterone responsiveness of genetically hypertensive rats, we compared characteristics of renal cytosolic aldosterone receptors from the M strain of stroke-prone, spontaneously hypertensive rats (M-SHRSP) with normotensive Wistar-Kyoto rats (WKY). In M-SHRSP, blood pressure was elevated significantly at 6 wk of age, when their plasma aldosterone concentrations were similar to those in WKY. Decreases in urine volume and sodium excretion were also observed in M-SHRSP. At 10 wk of age, M-SHRSP plasma aldosterone concentrations became significantly higher than those in WKY. On the other hand, the concentration of renal cytosolic aldosterone receptors (type I, aldosterone specific) had already increased at 6 wk of age in M-SHRSP, with no difference in affinity, and levels remained increased thereafter. There were no significant differences in molecular weights or ionic charges of either "activated" or "non-activated" aldosterone-receptor complexes between M-SHRSP and WKY, indicating that the molecular properties were similar in both groups. These results suggest that the increased concentration of aldosterone receptors in the kidneys of M-SHRSP might increase their aldosterone responsiveness and contribute to the development of high blood pressure in these animals.